Editorial Compilation—Part XVIII

Welcome to the latest issue of “Seminars in Thrombosis and Hemostasis (STH)” published under the “banner” of “Editorial Compilation,” this being the 18th such issue ([Table 1]). Historically, “STH” is a theme-driven publication; however, ongoing opportunities emerge to disseminate wide-ranging contributions of current interest or controversy, which do not directly suit an ongoing themed issue. We also require a medium to enable publication of peer-reviewed “unsolicited” manuscripts if accepted, as well as contributions from our Eberhard F. Mammen Young Investigator Award winners (see [Table 2] for previous Editorials related to the Eberhard F. Mammen awards). As is now standard for this compilation series, this study contains a mixture of articles that comprise the above elements, as well as broadly fitting within the standard themes of “thrombosis” and “bleeding.”

Table 1 Past STH issues in the series “editorial compilation”

1. Favaloro EJ, Lippi G. Editorial compilation I. Semin Thromb Hemost. 2016 Feb;42(1):5–8

2. Favaloro EJ, Lippi G. Editorial compilation II. Semin Thromb Hemost. 2016 Sep;42(6):599–602

3. Favaloro EJ, Lippi G. Editorial compilation III. Semin Thromb Hemost. 2017 Feb;43(1):4–7

4. Favaloro EJ, Lippi G. Editorial compilation IV. Semin Thromb Hemost. 2017 Sep;43(6):549–552

5. Favaloro EJ, Lippi G. Editorial compilation V. Semin Thromb Hemost. 2018 Apr;44(3):193–196

6. Favaloro EJ, Lippi G. Editorial compilation VI. Semin Thromb Hemost. 2019 Feb;45(1):5–9

7. Favaloro EJ, Lippi G. Editorial compilation VII. Semin Thromb Hemost. 2019 Jul;45(5):429–432

8. Favaloro EJ, Lippi G. Editorial compilation VIII. Semin Thromb Hemost. 2020 Jun;46(4):393–397

9. Favaloro EJ, Lippi G. Editorial compilation IX. Semin Thromb Hemost. 2021 Feb;47(1):6–10

10. Favaloro EJ, Lippi G. Editorial compilation X. Semin Thromb Hemost. 2021 Oct 47(7):754–758

11. Favaloro EJ, Lippi G. Editorial compilation XI. Semin Thromb Hemost. 2022 Mar;48(2):127–131

12. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation XII. Semin Thromb Hemost. 2022 Jul;48(5):497–501

13. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation XIII. Semin Thromb Hemost. 2023 Jul;49(5):427–432

14. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation XIV. Semin Thromb Hemost. 2024 Mar; 50(2):151–156

15. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation-XV. Semin Thromb Hemost. 2024 Jun;50(4):521–526

16. Vu HH, McCarty OJT, Favaloro EJ. Contact activation: where thrombosis and hemostasis meet on a foreign surface, plus a mini-editorial compilation (“part XVI”). Semin Thromb Hemost. 2024 Oct;50(7):933–936

17. Favaloro EJ, Pasalic L, Fan BE, Lippi G. Editorial compilation-XVII. Semin Thromb Hemost. 2025 Jun;51(5):475–480

Table 2 Past STH editorials related to Eberhard F. Mammen award announcements

1. Favaloro EJ. Welcome to a special issue of Seminars in Thrombosis and Hemostasis—the closing issue for 2008. Semin Thromb Hemost 2008; 34: 693–696

2. Favaloro EJ. A Tribute to Eberhard F. Mammen, M.D. (1930–2008). Semin Thromb Hemost 2008; 34: 703–708

3. Favaloro EJ. Welcome to the first issue of Seminars in Thrombosis and Hemostasis for 2009. Semin Thromb Hemost 2009; 35:1–2

4. Favaloro EJ. Winners of the Inaugural Eberhard F. Mammen Award for most popular article. Semin Thromb Hemost 2009; 35: 587–590

5. Favaloro EJ. Editorial. 2009 Eberhard F. Mammen Young Investigator Award Winners. Semin Thromb Hemost 2010; 36: 469–470

6. Favaloro EJ. Winners of the 2010 Eberhard F. Mammen award for most popular article during 2008–2009. Semin Thromb Hemost. 2010;36(7):685–692

7. Favaloro EJ. 2011 Eberhard F. Mammen award announcements. Semin Thromb Hemost. 2011;37(5):431–439

8. Favaloro EJ. 2012 Eberhard F. Mammen award announcements. Semin Thromb Hemost. 2012;38:425–432

9. Favaloro EJ. 2013 Eberhard F. Mammen award announcements. Semin Thromb Hemost. 39:567–574

10. Favaloro EJ. 2014 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2014;40(4):407–412

11. Favaloro EJ. 2014 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2014;40(7):718–723

12. Favaloro EJ. 2015 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2015;41(7):673–679

13. Favaloro EJ. 2015 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2015;41(8):809–815

14. Favaloro EJ. 2016 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2016;42(4):325–330

15. Favaloro EJ. 2016 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2017;43(3):235–241

16. Favaloro EJ. 2017 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2017;43(4):357–363

17. Favaloro EJ. 2017 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2018;44(2):81–88

18. Favaloro EJ. 2018 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2018;44(3):185–192

19. Favaloro EJ. 2018 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2019;45(2):123–129

20. Favaloro EJ. 2019 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2019;45(3):215–224

21. Favaloro EJ. 2019 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost 2020;46(2):105–113

22. Favaloro EJ. 2020 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2020;46(4):383–392

23. Favaloro EJ. 2020 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost 2021;46(3): 229–237

24. Favaloro EJ. 2021 Eberhard F. Mammen Award Announcements: Part I—Most Popular Articles. Semin Thromb Hemost. 2021 Jul;47(5):467–476

25. Favaloro EJ. 2021 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2022 Apr;48(3):265–273

26. Favaloro EJ. 2022 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2022 Jul;48(5):502–513

27. Favaloro EJ. 2023 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2023 Jul;49(5):417–426

28. Favaloro EJ. 2022 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2023 Nov;49(8):775–782

29. Favaloro EJ. 2024 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2024 Oct;50(7):919–932

30. Favaloro EJ. 2023 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2024 Nov;50(8):1049–1057

31. Favaloro EJ. 2024 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2025 Jun;51(5):481–449

This issue begins with a review on disseminated intravascular coagulation (DIC) by Iba et al,[1] who introduce the readers of STH to the new definition and diagnostic criteria recently released by the International Society on Thrombosis and Haemostasis. The new guidance reflects advances in understanding the pathophysiology of DIC, which is now defined as an acquired, life-threatening condition involving systemic coagulation activation, impaired fibrinolysis, and endothelial injury. The revised framework emphasizes the condition's dynamic nature, progressing from preclinical abnormalities to overt clinical manifestations such as bleeding and (multiple) organ dysfunction. A major innovation in the 2025 update is the phase-based classification of DIC: pre-DIC, early phase DIC, and overt DIC. Early phase DIC—also referred to as subclinical or compensated DIC—is characterized by laboratory abnormalities preceding clinical symptoms. Overt DIC represents the advanced stage with clear evidence of coagulopathy and organ failure. Importantly, the new criteria are tailored to the underlying disease, such as sepsis, trauma, or malignancy. For example, the sepsis-induced coagulopathy score is now acknowledged as a tool for detecting early-phase DIC in septic patients. The overt DIC scoring system has been refined, including revised D-dimer thresholds: levels >3× and >7× the upper normal limit now corresponding to 2 and 3 points, respectively. Platelet count, prothrombin time-International Normalized Ratio, and fibrinogen levels remain key indicators. The criteria also classify DIC into thrombotic and hemorrhagic phenotypes. Thrombotic DIC is marked by microvascular thrombosis and organ dysfunction, while hemorrhagic DIC is characterized by bleeding due to consumption of coagulation factors. By introducing clearer definitions and individualized approaches, these updates aim to enable earlier diagnosis and more effective management of DIC across clinical contexts.

Next, Østergaard et al explore the mechanisms of hypercoagulability in thrombotic antiphospholipid syndrome (APS) with a focus on human studies.[2] Thrombosis is the most common manifestation of APS, but concurring evidence of the mechanisms leading to a hypercoagulable state and thereby thrombosis is lacking. Existing reviews on this topic often include both animal and in vitro models. Additionally, studies with a systematic approach and stringent methodology, focusing exclusively on human studies, are lacking. Therefore, the authors conducted a scoping review of studies with human subjects, focusing on the mechanisms contributing to hypercoagulability in thrombotic APS (TAPS). The process was guided by the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) Extension for Scoping Reviews and performed according to a preregistered protocol in Open Science Framework. A systematic search of Ovid (EMBASE) and MEDLINE (PubMed) was performed. Records investigating mechanisms of hypercoagulability in adults (≥18 years) with TAPS, published between January 2000 and October 2024, were included. A total of 4,160 titles and abstracts were screened, 115 articles were assessed in full text, of which 35 studies fulfilled the predefined eligibility criteria for inclusion. Of the included studies, eight focused on primary hemostasis, 10 on secondary hemostasis, nine on fibrinolysis, four on neutrophil extracellular traps (NETs), six on endothelial cells, three on complement factors, five on monocytes, three on oxidized low-density lipoprotein complexes, two on oxidative stress, and one on amyloid-β1–40. No clear consensus was found regarding the underlying cause of hypercoagulability in TAPS, highlighting the need for further studies with human subjects. Nonetheless, the scoping review indicates that hypercoagulability in TAPS is possibly multifactorial, with no single mechanism being solely responsible.

This issue of STH continues with a review on the risks and benefits of nonsteroidal anti-inflammatory drugs (NSAIDs) in the hemostatic system by Cignarella et al.[3] Chronic use of multiple drugs increases the risk of adverse drug reactions, drug interactions, and poor therapeutic adherence. In elderly or frail patients, some drugs may become ineffective or even harmful with advancing age and worsening clinical conditions. NSAIDs have been extensively used for decades and, as a class, are often inappropriately prescribed and involved in polypharmacotherapy, with untoward effects. In view of the dynamic and mutual relationship between inflammation and hemostasis in various clinical scenarios, the use of anti-inflammatory agents, including NSAIDs, may tip this difficult balance in patients with hemostatic disorders. Rather than on well-established actions such as the clinically relevant antiplatelet action of low-dose aspirin and gastrointestinal bleeding, this review focuses on less highlighted, emerging, or sometimes overlooked NSAID efficacy and safety endpoints. For instance, preclinical studies suggest that the antiplatelet action of low-dose aspirin enhances immune system activity against cancer cells, thereby preventing metastasis. While use of NSAIDs in patients with coagulation disorders may have an acceptable risk-to-benefit ratio in selected patients, clinical judgement is required, especially in cases of renal impairment that can be worsened by NSAIDs or in cases with high bleeding risk, such as in hemophilia. In the context of polypharmacotherapy, attenuation of aspirin antiplatelet action by concomitant and inaccurately timed ibuprofen treatment may undermine the clinical benefit of aspirin in cardiovascular prevention. Thus, collaborative cross-disciplinary efforts of pharmacologists and clinicians would be desirable to enhance appropriateness, efficacy, and safety of NSAID treatment in different settings of care.

Next, Petrou et al review the ABO blood system in relation to hemostasis and thrombosis.[4] The relationship between non-O blood groups and thromboembolic events has been suggested by several studies, although the exact underlying mechanisms are not fully elucidated. However, the correlation between ABO blood groups with the opposite pole of hemostasis, hemorrhage, has been investigated less thoroughly. Non-O blood groups confer an overall increased risk of single, recurrent, and provoked thromboembolic episodes. On the other hand, blood group O has been associated with more severe bleeding events and less favorable manifestations in individuals with hemorrhagic disorders. Therefore, ABO blood group screening may play a role in assessing both thrombotic and hemorrhagic risks and could potentially be incorporated into existing clinical prediction systems. This strong belief is supported by the ongoing research. Nevertheless, to date, the majority of studies exhibit significant heterogeneity, and given the prevalence of non-O blood groups, a natural reluctance to incorporate blood groups into risk assessment models arises. Therefore, a more targeted approach should be considered to provide safe outcomes. The in vitro estimation of the thrombotic and hemorrhagic profile of each blood group separately, the quantitative estimation of von Willebrand factor and factor VIII level and activity, together with platelet function in several disease settings and in well-organized studies, could be useful to establish a clear relationship of ABO blood types with hemostatic and thrombotic disorders. This approach ensures a safe method for categorizing a patient's risk, managing treatment, and influencing prognosis.

Sokou et al then review platelet and plasma transfusion strategies for neonates, assessing the evidence, guidelines, and addressing unanswered questions.[5] The transfusion of platelets and fresh frozen plasma (FFP) to critically ill neonates in neonatal intensive care units is a common intervention, yet it is still widely performed without adhering to international guidelines. The guidance itself on the therapeutic management of neonatal coagulation disorders is generally limited due to the absence of strong indications for treatment and is mainly aimed at preventing major hemorrhagic events, such as intraventricular hemorrhage in premature neonates. Historically, the under-representation of neonates in clinical studies related to transfusion medicine has led to significant gaps in knowledge regarding the best transfusion practices in this vulnerable group and to a wide variability in policies among different neonatal units, often based on local experience or guidance designed for older children or adults, and possibly increasing the risk of inappropriate or ineffective interventions. Platelet transfusion and, in particular, FFP administration have been linked to potentially fatal complications in neonates, so that any decision needs to be carefully balanced and requires a thorough consideration of multiple factors in the neonatal population. Despite recent advances toward more restrictive practices, platelet and FFP transfusions are still subject to wide variability in practice.

A review on neutrophils and NETs is then presented by Hassani et al.[6] The authors remind us that neutrophils are astonishing cells involved in nonspecific immunity, especially against bacterial and fungal infections. Their half-life is short, but despite their important role in nonspecific immunity, they defend the host even after their death by providing secondary structures such as NETs, which reflect a network comprising DNA, histones, and proteins, including elastase, cathepsin G, and myeloperoxidase. In this context, in addition to their primary role in hemostasis, NETs also play a role in thrombosis, an area that has perhaps received less attention. Nonetheless, NETs can promote both venous and arterial thrombus formation (immuno-thrombosis) by their effects on primary and secondary hemostasis. Their participation in thrombus formation includes the release of microparticles and components of the inflammasome. Neutrophils, in interaction with other cells, including platelets, can further contribute to thrombosis. Activated platelets can capture neutrophil-derived microparticles containing tissue factor (TF), leading to TF accumulation and increased fibrin deposition. Furthermore, neutrophil inflammasomes, as a regulator of the generation of IL-1 family proteins, have been shown to boost thrombosis formation in response to hypoxia. Overall, understanding the complex and reciprocal effects of neutrophils with other hemostasis-related cells and components provides important insights into hemostatic mechanisms, and this may open avenues in medical research and potential therapeutic interventions.

The review by Huang et al[7] is also focused on NETS, but this time in relation to their use as a strategy for treating acute ischemic stroke (AIS) based on thrombolysis resistance. AIS is a life-threatening thrombotic disorder, with intravenous thrombolysis serving as the first-line treatment during its acute phase. However, thrombolysis resistance diminishes the success rate of early reperfusion. Recent studies have highlighted NETs as a critical factor contributing to thrombolysis resistance. Targeting NETs with deoxyribonuclease I has been shown to significantly improve the thrombolytic efficacy of recombinant tissue plasminogen activator and reduce the risk of hemorrhagic transformation. In this review, the authors summarize current knowledge on the mechanisms by which NETs contribute to thrombosis and thrombolysis resistance, explore the prospective and feasibility of targeting NETs to improve thrombolysis, and provide information about the creation of innovative thrombolytic treatment approaches for AIS.

The last review in this issue of STH is by Kalantari et al, who review thrombocytopenia after hematopoietic stem cell transplantation (HSCT) in both pediatric and adult patients.[8] Thrombocytopenia following HSCT is a common complication that is associated with a remarkable increase in morbidity and mortality. Post-HSCT thrombocytopenia is a multifactorial condition with several mechanisms, including reduced platelet production in bone marrow, immune-mediated platelet destruction, and consumptive thrombocytopenia. Graft-versus-host disease, medications, infections, and autoimmune mechanisms are potential risk factors for post-HSCT thrombocytopenia. Management of post-HSCT thrombocytopenia primarily focuses on supportive care through platelet transfusions. Moreover, immunosuppressive agents are used to target immune-mediated mechanisms. Thrombopoietin receptor agonists and complement inhibitors are novel treatment options with promising results and fewer side effects. However, further research is essential for establishing treatment protocols and improving patient care. In this review, we provide a better understanding of the pathophysiology and risk factors associated with post-HSCT thrombocytopenia for early detection and intervention, ultimately aiming to reduce complications.

The issue continues with two Commentaries. First, Iba et al outline the evolution of clinical trials in anticoagulation for sepsis.[9] Demonstrating the efficacy of new treatments in any condition may be a challenging endeavor, and this is particularly the case in sepsis. In the early 21st century, recombinant activated protein C showed a survival benefit in severe sepsis. Nevertheless, subsequent studies could not replicate these results, leading to the discontinuation of this agent. Several potential reasons have been proposed for the unfavorable results of trials, including the selection of an inappropriate outcome target. Concerning anticoagulant therapies, some studies have targeted sepsis with DIC and demonstrated clinical benefits, while other studies have focused on severe sepsis or septic shock independent of whether patients had DIC. The timing for treatment initiation, dosage, and duration of anticoagulant agents could be significant factors contributing to the limitations faced in these trials. Moreover, relying solely on 28-day mortality as the primary endpoint for sepsis trials may not be appropriate, as it can be influenced by various factors beyond anticoagulant therapies, and discernment in a shorter period might be more pertinent. Success in clinical trials is more likely if these issues are addressed and improvements are made. Recent clinical trials, focusing on anticoagulants, are increasingly targeting sepsis or septic shock with coagulopathy and adopting composite endpoints, including DIC resolution, to overcome some of these challenges.

The second Commentary is by Fan et al, who ask: did the COVID-19 (coronavirus disease 2019) pandemic push direct oral anticoagulants (DOACs) ahead of vitamin K antagonists such as warfarin? The COVID-19 pandemic introduced unprecedented disruptions to health care delivery, compelling rapid adaptations in anticoagulation management. DOACs, already displacing warfarin due to their convenience[10] and reduced monitoring requirements, appeared well-positioned for broader adoption during pandemic-induced lockdowns. This commentary examines whether the pandemic catalyzed a meaningful shift in anticoagulant prescribing patterns from VKAs to DOACs, drawing on data from the United Kingdom, Australia, the United States, Europe, and Asia. In the United Kingdom, national guidance led to a sudden and large-scale shift to DOACs, with sustained changes following the pandemic. In contrast, Australia and the United States exhibited continuity in preexisting trends, with modest, transient shifts that did not persist. Asian and European data revealed a gradual trajectory toward DOACs, likely driven by long-term policy and infrastructure rather than acute pandemic pressures. The authors conclude that while no universal transformation occurred, the pandemic accentuated existing preferences and exposed system-level vulnerabilities in warfarin monitoring. The global experience also suggests that the COVID-19 crisis served as a selective accelerant of DOACs adoption, where health care systems and policies facilitated change. As health systems prepare for future disruptions, ensuring equitable access to DOACs and investing in remote care infrastructure will be essential to maintaining continuity and safety in anticoagulation therapy.

This issue of STH concludes with several letters to the editor or correspondence. First, Sattler et al describe a case of long-term anticoagulation in a severe hemophilia A patient receiving efanesoctocog α prophylaxis.[11] Next, Shimomura et al describe twins with hemophilia B in which the co-occurrence of low-frequency pathogenic variants in the platelet “TBXA2R” gene exacerbated their hemorrhagic symptoms.[12] Finally, Villa et al discuss the value of “JAK2” V617F mutation screening for peripheral arterial thrombosis.[13]

As always, we once again thank all the authors of this latest issue of “Editorial Compilations” for their original and comprehensive contributions, and we hope our readership enjoys this latest instalment in this series.

Finally, in the previous compilation issue,[14] we issued a reminder that STH had transitioned to an online submission system (https://mc.manuscriptcentral.com/sth). Thus, if any reader is interested in submitting a manuscript, they should do so at this website. In this study, we provide an update on some metrics around submission and acceptance rates through the new system, and also in comparison with the past.[15]

• References

• 1 Iba T, Maier CL, Scarlatescu E, Levy JH. Introducing the new definition and diagnostic criteria of disseminated intravascular coagulation released by the International Society on Thrombosis and Haemostasis in 2025. Semin Thromb Hemost 2026; 52 (01) 10-17
• 2 Østergaard SED, Hansen RS, Voss A, Bor MV. Exploring the mechanisms of hypercoagulability in thrombotic antiphospholipid syndrome: a scoping review of human studies. Semin Thromb Hemost 2026; 52 (01) 18-34
• 3 Cignarella A, Campello E, Ramaschi GE, Simion C, Simioni P. Risks and benefits of nonsteroidal anti-inflammatory drugs in the hemostatic system. Semin Thromb Hemost 2026; 52 (01) 35-45
• 4 Petrou E, Donta AM, Mellou S, et al. The ABO blood system and associated implications for hemostasis and thrombosis. Semin Thromb Hemost 2026; 52 (01) 46-55
• 5 Sokou R, Gounari EA, Lianou A. et al. Rethinking platelet and plasma transfusion strategies for neonates: evidence, guidelines, and unanswered questions. Semin Thromb Hemost 2026; 52 (01) 56-76
• 6 Hassani S, Fazeli A, Dorgalaleh A. et al. Neutrophil-mediated effects on hemostasis and thrombosis: unraveling their complex interaction in thrombotic events. Semin Thromb Hemost 2026; 52 (01) 92-105
• 7 Huang G, Wu H, Lin B. et al. Targeting neutrophil extracellular traps: a new strategy for the treatment of acute ischemic stroke based on thrombolysis resistance. Semin Thromb Hemost 2026; 52 (01) 80-91
• 8 Kalantari A, Karimizadeh Z, Jafari L, Behfar M, Hamidieh AA. Thrombocytopenia after hematopoietic stem cell transplantation in pediatrics and adults: a narrative review including etiology, management, monitoring, and novel therapies. Semin Thromb Hemost 2026; 52 (01) 106-125
• 9 Iba T, Helms J, Maier CL, Ferrer R, Levy JH. Evolution of clinical trials in anticoagulation for sepsis: bridging past to future. Semin Thromb Hemost 2026; 52 (01) 126-138
• 10 Fan BE, Tan JHM, Tan DS. COVID-19 and anticoagulant use: did the pandemic push DOACs ahead of warfarin?. Semin Thromb Hemost 2026; 52 (01) 139-143
• 11 Sattler L, Herb A, Gerout AC. et al. Long-term anticoagulation in a severe hemophilia a patient receiving efanesoctocog alpha prophylaxis: a case report. Semin Thromb Hemost 2026; 52 (01) 144-147
• 12 Shimomura M, Mizoguchi Y, Kajihara K. et al. The co-occurrence of low-frequency pathogenic variants in TBXA2R exacerbating the hemorrhagic symptoms in siblings with hemophilia B. Semin Thromb Hemost 2026; 52 (01) 148-153
• 13 Villa A, Bravetti C, Gauthier N. et al. JAK2 V617F mutation screening for peripheral arterial thrombosis. Semin Thromb Hemost 2026; 52 (01) 154-159
• 14 Favaloro EJ, Pasalic L, Fan BE, Lippi G. Editorial compilation-XVII. Semin Thromb Hemost 2025; 51 (05) 475-480
• 15 Favaloro EJ. Welcome to seminars in thrombosis & hemostasis 2026. Semin Thromb Hemost 2026; 52 (01) 6-9

Publication History

Article published online:
13 January 2026